PMID- 27780541
OWN - NLM
STAT- MEDLINE
DCOM- 20180112
LR  - 20180503
IS  - 1532-3102 (Electronic)
IS  - 0143-4004 (Linking)
VI  - 47
DP  - 2016 Nov
TI  - ATF3 is a negative regulator of inflammation in human fetal membranes.
PG  - 63-72
LID - S0143-4004(16)30525-2 [pii]
LID - 10.1016/j.placenta.2016.09.006 [doi]
AB  - INTRODUCTION: Infection and inflammation stimulate pro-inflammatory cytokines, 
      prostaglandins and matrix metalloproteinase (MMP)-9, which play a central role in 
      myometrial contractions and rupture of fetal membranes. In human and mouse immune 
      cells, activating transcription factor 3 (ATF3) is a negative regulator of 
      inflammation. No studies have examined the role of ATF3 in human labour. METHODS: 
      Primary amnion cells were used to determine the effect of interleukin (IL)-1beta and 
      the bacterial product fibroblast-stimulating lipopeptide (fsl-1) on ATF3 
      expression, and the effect of ATF3 siRNA on pro-labour mediators. ATF3 expression 
      was assessed in fetal membranes from non-labouring and labouring women at term 
      and preterm, and after preterm pre-labour rupture of membranes (PPROM). RESULTS: 
      IL-1beta and fsl-1 significantly increased ATF3 expression. Silencing ATF3 
      significantly increased IL-1beta- or fsl-1-induced expression of pro-inflammatory 
      cytokines (TNF-alpha, IL-1alpha, IL-1beta, IL-6) and chemokines (IL-8 and monocyte 
      chemoattractant protein-1 (MCP-1)); cyclooxygenase-2 (COX-2) mRNA expression and 
      prostaglandin PGF(2alpha) release; and MMP-9 expression. ATF3 expression was 
      decreased in fetal membranes with term labour. There was no effect of preterm 
      labour or PPROM on ATF3 expression. DISCUSSION: ATF3 is a negative regulator of 
      inflammation in human fetal membranes; in primary amnion cells, ATF3 expression 
      is induced by IL-1beta and fsl-1, and ATF3 silencing further exacerbates the 
      inflammatory response when stimulated with these factors. Subsequently, ATF3 
      expression is decreased in fetal membranes after term labour and with preterm 
      chorioamnionitis, conditions closely associated with inflammation and infection. 
      Our data suggest that ATF3 may play a role in the terminal processes of human 
      labour and delivery.
CI  - Copyright (c) 2016 Elsevier Ltd. All rights reserved.
FAU - Lim, Ratana
AU  - Lim R
AD  - Obstetrics, Nutrition and Endocrinology Group, Department of Obstetrics and 
      Gynaecology, University of Melbourne, Victoria, Australia; Mercy Perinatal 
      Research Centre, Mercy Hospital for Women, Heidelberg, Victoria, Australia.
FAU - Barker, Gillian
AU  - Barker G
AD  - Obstetrics, Nutrition and Endocrinology Group, Department of Obstetrics and 
      Gynaecology, University of Melbourne, Victoria, Australia; Mercy Perinatal 
      Research Centre, Mercy Hospital for Women, Heidelberg, Victoria, Australia.
FAU - Liong, Stella
AU  - Liong S
AD  - Obstetrics, Nutrition and Endocrinology Group, Department of Obstetrics and 
      Gynaecology, University of Melbourne, Victoria, Australia; Mercy Perinatal 
      Research Centre, Mercy Hospital for Women, Heidelberg, Victoria, Australia.
FAU - Nguyen-Ngo, Caitlyn
AU  - Nguyen-Ngo C
AD  - Obstetrics, Nutrition and Endocrinology Group, Department of Obstetrics and 
      Gynaecology, University of Melbourne, Victoria, Australia; Mercy Perinatal 
      Research Centre, Mercy Hospital for Women, Heidelberg, Victoria, Australia.
FAU - Tong, Stephen
AU  - Tong S
AD  - Mercy Perinatal Research Centre, Mercy Hospital for Women, Heidelberg, Victoria, 
      Australia; Translational Obstetrics Group, Department of Obstetrics and 
      Gynaecology, University of Melbourne, Victoria, Australia.
FAU - Kaitu'u-Lino, Tu'uhevaha
AU  - Kaitu'u-Lino T
AD  - Mercy Perinatal Research Centre, Mercy Hospital for Women, Heidelberg, Victoria, 
      Australia; Translational Obstetrics Group, Department of Obstetrics and 
      Gynaecology, University of Melbourne, Victoria, Australia.
FAU - Lappas, Martha
AU  - Lappas M
AD  - Obstetrics, Nutrition and Endocrinology Group, Department of Obstetrics and 
      Gynaecology, University of Melbourne, Victoria, Australia; Mercy Perinatal 
      Research Centre, Mercy Hospital for Women, Heidelberg, Victoria, Australia. 
      Electronic address: mlappas@unimelb.edu.au.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20160914
PL  - Netherlands
TA  - Placenta
JT  - Placenta
JID - 8006349
RN  - 0 (ATF3 protein, human)
RN  - 0 (Activating Transcription Factor 3)
RN  - 0 (Cytokines)
RN  - 0 (Diglycerides)
RN  - 0 (FSL-1 lipoprotein, synthetic)
RN  - 0 (Interleukin-1beta)
RN  - 0 (Oligopeptides)
SB  - IM
MH  - Activating Transcription Factor 3/genetics/*metabolism
MH  - Cell Line
MH  - Chorioamnionitis/metabolism
MH  - Cytokines/genetics/metabolism
MH  - Diglycerides/pharmacology
MH  - Extraembryonic Membranes/drug effects/*metabolism
MH  - Female
MH  - Fetal Membranes, Premature Rupture/genetics/*metabolism
MH  - Humans
MH  - Inflammation/*metabolism
MH  - Interleukin-1beta/pharmacology
MH  - Labor, Obstetric/metabolism
MH  - Oligopeptides/pharmacology
MH  - Pregnancy
OTO - NOTNLM
OT  - ATF3
OT  - Fetal membranes
OT  - Human labour
OT  - Infection
OT  - Inflammation
EDAT- 2016/10/27 06:00
MHDA- 2018/01/13 06:00
CRDT- 2016/10/27 06:00
PHST- 2016/07/18 00:00 [received]
PHST- 2016/09/07 00:00 [revised]
PHST- 2016/09/13 00:00 [accepted]
PHST- 2016/10/27 06:00 [pubmed]
PHST- 2018/01/13 06:00 [medline]
PHST- 2016/10/27 06:00 [entrez]
AID - S0143-4004(16)30525-2 [pii]
AID - 10.1016/j.placenta.2016.09.006 [doi]
PST - ppublish
SO  - Placenta. 2016 Nov;47:63-72. doi: 10.1016/j.placenta.2016.09.006. Epub 2016 Sep 
      14.